1. Preventing long term complications of paraplegia
William Desloges, MD
Orthopaedic Surgery Department
University of Ottawa

2. Outline Introduction Complications of paraplegia Conclusion
Pressure Ulcers
Pulmonary Complications
Osteoporosis and Fractures
Urinary Tract Dysfunction
Neurogenic Heterotopic Ossification
Spasticity
Venous thrombosis
Upper extremity arthropathies
Bowel Complications
Cardiovascular Diseases
Neuropathic/Spinal cord pain
Conclusion

3. Introduction: Paraplegia
Causes
Spinal cord lesions below T1 level
Complete or incomplete
Complications
Morbidity and mortality
Quality of life
Multidisciplinary management
Orthopaedic Spine Surgeon

4. Pressure Ulcers

5. Pressure Ulcers (Regan et al 2009)
The cost of accelerated wound treatment to heal a stage III ulcer in a community- dwelling paraplegic over a 3 months period has been estimated at $27,632 Cdn.
Among patients with SCIs, annual incidence rates of pressure ulcer range from 20-31%, and the prevalence rates from 10.2% to 30%.
In community-dwelling persons with SCI, 25% of pressure ulcers
are classified as severe (stage III or IV).2 Another type of
pressure ulcer is suspected deep tissue injury. This injury looks
like a bruise on intact skin but may rapidly progress to involve
deeper layers, despite treatment.8,15
Cost data on pressure ulcers in SCI populations are dif-
ficult to obtain.16 In a case study of a community-dwelling
person with paraplegia, Allen and Houghton16 demonstrated
that the cost of 3 months of accelerated wound treatment to
heal a stage III ulcer was $27,632 Canadian, with approximately
half the cost paid for by the person. In the United
Annual incidence rates range from 20% to 31% and prevalence
rates from 10.2% to 30%.11,17

6. Pressure Ulcers (Regan et al 2009)
Risk factors:
Limitations in activity and mobility
Injury completeness
Moisture from bowel and/or urinary incontinence
Lack of sensation
Muscle atrophy
Nutritional status
Prevention of pressure ulcers requires the recognition of
significant risk factors, which effect either the intensity and
duration of pressure or the tissue tolerance for pressure.20
Identified risk factors include limitations in activity and mobility,
injury completeness, moisture from bowel and/or bladder
incontinence, lack of sensation, muscle atrophy, nutritional
status, and being underweight.11,17,19

7. Pressure Ulcers Prevention Strategies
Pressure relief practices:
On average, it takes ~ 2 minutes of pressure relief to raise the transcutaneous oxygen tension to normal levels (Coggrave et al 2003)
Effective pressure relieving techniques for paraplegic patients unable to perform manual weight shift include (Henderson et al 1994)
Forward leaning position: 78% reduction in ischial tuberosity pressure as compared to neutral sitting position
65° tipped back position: 47% reduction in ischial tuberosity pressure as compared to neutral sitting position
Leaning side to side
Doing a pressure relief lift for > 2 minutes
Neuromuscular Electrical Stimulation:
(Level 4 evidence) Electrical stimulation increases regional blood flow thereby assisting in prevention of pressure ulcers (Regan et al 2009)
Pressure relief practices: The techniques chosen for pressure relief depend on
the physical and cognitive status of the individual. When a
manual weight shift cannot be performed, 1 alternative is a
mechanical reclining or power tilt wheelchair. It has been
suggested that pressure relief optimally should be performed
every 15 to 30 minutes for 30 to 120 seconds, depending on the
technique1 (table 5).
A retrospective chart review of 46 subjects with an SCI seen
in a seating clinic noted that approximately 2 minutes of
pressure relief was required to raise transcutaneous oxygen
tension to unloaded levels for most subjects.36 The required
duration of pressure relief was more easily sustained by the
These findings suggest that a forward-leaning position is the
most effective pressure relief technique, if sustained for an
appropriate period. Leaning side to side, having the wheelchair
tipped back by 65° or more, or doing a pressure relief lift for an
appropriate length of time (ie, 2min) also was effective. The
When the subjects were in a forward-leaning and 65° tipped- back position, there was a statistically significant pressure
reduction at the IT and over the circumscribed area (forward
lean: 78% reduction at IT, 70% reduction over circumscribed
area [P.05]; 65° tipped back: 47% reduction at IT, 36%
reduction over circumscribed area [P.05]); this compared
with a 27% reduction at the IT, and to a 17% reduction over the
circumscribed area (P.05) in the 35° tipped-back position.
While the pressure reduction for the 65° tipped-back position
Because of its easy handling and its good amicability, electrostimulation of the gluteal region - one of the most common localisations of pressure-caused ulcers - by means of an anal electrode might be put to good effect even in prophylaxis in the treatment of paraplegic patients. (Lippert-Grüner M.)
Research also has shown that, with increasing interface
pressures over bony prominences, regional blood flow is adversely
affected.9,30 Electrical stimulation has been shown to
change blood flow to skin and muscle. It is believed that, by
increasing regional blood flow, tissue viability is enhanced,
thereby assisting with pressure ulcer prevention9,18,32-34 (table 4).
Mawson et al35 administered HVPGS to 29 subjects lying

8. Pressure Ulcers Prevention Strategies
Wheelchair Cushion
Materials: static (gel, foam, water) vs dynamic (air-filled bladders)
Shape
Temperature effects: Higher temperatures increase tissue susceptibility (Foam)
Specialized pressure mapping assessment to account for interindividual differences in pressure contact areas
Lumbar Support
Varying lumbar support thickness was found to have negligible effect on reducing seated buttock pressures at the Ischial Tuberosity (Shields et al 1992)
There is level 3 evidence that adding lumbar support to the
wheelchair of those with a chronic SCI has a negligible effect on
reducing seated buttock pressures at the IT. As a consequence, it
is unlikely to have a role in pressure ulcer prevention post-SCI.

9. Pressure Ulcers Prevention Strategies
Seating Clinics and Education
Have been shown to reduce the incidence of pressure ulcers when incorporated in rehabilitation programs (Dover 1992)
Emphasize personal responsibility for skin care, make recommendation for appropriate seating system, and give on going feedback to patients
Education regarding the prevention of pressure ulcers post-
SCI includes an emphasis on taking personal responsibility for
maintaining healthy skin through personal care, inspection of
skin, pressure relief, and the correct use of prescribed equipment.
9 The incorporation of seating clinics into both inpatient
and outpatient rehabilitation programs has been shown to reduce
the incidence of pressure ulcers and readmission rates as
a result of pressure ulcers.45 Seating clinics not only provide
education but also make recommendations for appropriate seating
systems based on interface pressures, thermography, and
assessments of tissue viability. Verbal and visual feedback are
provided to the individual with an SCI, and active participation
is encouraged36,45,46 (table 8).

10. Osteoporosis and Fractures

11. Osteoporosis and Fractures
In paraplegia, osteoporosis affects the pelvis and lower extremities; sublesional topography of demineralization
Radiological evidence of decreased bone mineral density and content can be detected in paralyzed limbs as early as 6 weeks post Spinal cord injury (Sheng-Dan et al 2006)
Cancellous bone is more affected than cortical bone
In the lower extremities, the trabecular metaphysical-epiphyseal areas of the proximal tibia and distal femur are most affected (Sheng-Dan et al 2006)
The paraplegic fracture: supracondylar femur fracture
Demirel et al. (1998) found a significant difference in bone mineral density when comparing patients with complete and incomplete lesions
Reduction in bone mineral density was found to be less in SCI patients with spasticity (Sheng-Dan et al 2006)
SCI induces bone loss, thereby increasing the fracture
risk. A decline in bone mineral density (BMD) and bone
mineral content (BMC) has been detected radiologically
in the paralyzed limbs of patients as early as 6 weeks
after SCI [1], and the dramatic reduction in BMD or
BMC has been amply documented in chronic SCI patients
[2, 3, 4, 5, 6, 7]. Osteoporosis generally involves the
pelvis and lower extremities in persons with paraplegia,
6 weeks after injury, respectively [6].
Cancellous bone more affected than cortical bone after SCI.
predominates
The most affected sites are the trabecular metaphysical-epiphyseal
areas of the distal femur and the proximal tibia.
Several factors appear to have an in.uence on bone
mass in SCI individuals. The level of the lesion and thus
the extent of impairment of motor and sensory function
may be taken into account .rst, because tetraplegics are
more likely to lose more bone mass throughout the
skeleton than paraplegics [9, 10, 15, 16] (Table 1,
Table 2). However, the similar severity of demineralization
in the sublesional area was shown between
paraplegics and tetraplegics, and the extent of the bone
loss may be variable [10, 13, 15]. In addition, bone mass
loss may be more severe in SCI individuals with complete
lesions (an absence of sensory or motor function
below the neurological level, including the lowest sacral
segment) than in those with incomplete lesions (partial
preservation of motor and/or sensory function below the
neurological level, including the lowest sacral segment)
[4, 9, 15, 17]. In a cross-sectional study of 11 patients
with complete SCI and 30 patients with incomplete SCI,
Demirel et al. [15] noticed a signi.cant di.erence in
BMD between the two groups of SCI patients. Osteopenia

12. Osteoporosis and Fractures
Age at the time of injury and duration since injury have been shown to affect bone mineral density
It is controversial as to whether or not a steady state in bone mineral density is achieved post SCI
Minor increase in BMD was observed in the humerus of paraplegic patients 1 year post injury (Dauty 2000)
Bone mass of the vertebral column is generally spared; rare to see compression fracture of vertebrae
Completeness of SCI is the single most important risk factor for pathological fractures among all modifiable and nonmodifiable risk factors. (Sheng-Dan et al 2006)

13. Osteoporosis and Fractures
(Sheng-Dan et al 2006)

14. Osteoporosis and Fractures: Prevention Strategies
Intensive exercise regime:
Contributed to preservation of upper extremity bone loss, but did not affect lower extremity bone loss in quadraplegics
Goemare et al. (1994) reported that standing may prevent bone loss in the region of the femoral shaft but not at the proximal hip
Pharmacological (Sheng-Dan et al 2006):
Calcium and Vitamin D supplementation does not prevent osteoporosis after SCI
Calcitonin has been shown to counteract early bone loss following SCI
RCTs using bisphosphonates have shown promising results in prevention of decreased mineral bone density in paraplegic patients; further studies required using higher doses.
Contrarily, Goemare et al. [102] reported that standing might partially prevent
bone loss in the region of the femoral shaft, but not at
the proximal hip.

15. Venous Thromboembolic Disease

16. Venous Thromboembolic Disease
The incidence of DVT has been reported to range between 9% and 90% in acute spinal cord injured patients (Aito et al. 2002)
Virchow’s triad: hypercoagulability, stasis, and intimal (venous inner wall) injury

17. Strong evidence supporting the use of LMWH in reducing venous thrombotic events
The use of heparin 5000 units sc Bid is no more effective than placebo as prophylaxis against DVT post-SCI.
Using a higher dose of unfractionated heparin than 5000 units Bid was found to be an effective DVT prophylactic, although it increased bleeding complications
Limited evidence to support nonpharmacological treatments such as sequential pneumatic compression devices or gradient elastic stockings
Given its predictability, dose-dependent plasma levels, long half-life, its low tendency to induce thrombocytopenia and reduced bleeding for a given antithrombotic effect, LMWH is the preferred prophylactic agent.
Conclusions: Twenty-three studies met inclusion criteria.
Thirteen studies examined various pharmacologic interventions
for the treatment or prevention of deep venous thrombosis in
patients with SCI. There was strong evidence to support the use
of low-molecular-weight heparin in reducing venous thrombosis
events, and a higher adjusted dose of unfractionated heparin
was found to be more effective than 5000 units administered every
12 hours, although bleeding complications were more common.
Nonpharmacologic treatments were also reviewed, but again limited
evidence was found to support these treatments.
Unfractionated heparin for prophylaxis: conclusions.
There is level 2 evidence (based on 1 low-quality RCT and 1
non-RCT) that 5000 IU of unfractionated heparin given subcutaneously
every 12 hours is no more effective than placebo
as prophylaxis against venous thrombosis post-SCI. There is
level 1 evidence (based on 1 RCT) that an adjusted (higher)
dose of subcutaneous heparin is more effective as prophylaxis
against venous thromboembolism than the administration of
5000 IU subcutaneous heparin every 12 hours; however, the
adjusted dose appears to be associated with a higher incidence
of bleeding complications.
Low-molecular-weight heparin for prophylaxis. LMWH
the use of sequential pneumatic compression devices or gradient
elastic stockings was associated with a reduced risk of a
diagnosed venous thromboembolism. Multivariate analysis
The clinical advantages of LMWH include its predictability,
dose-dependent plasma levels, long half-life, and reduced
bleeding for a given antithrombotic effect. Thrombocytopenia
has not been associated with the short-term use of LMWH.

18. Venous Thromboembolic Disease
Consensus is to discontinue prophylactic anticoagulants after 4 months as the risk of venous thromboembolism drops dramatically after 3–4 months (Gaber 2005).
Hypothesis (Gaber 2005):
Muscular spasticity
Arterial atrophy and reduced blood flow to the paralyzed lower limbs
Monitor patient for clinical signs and symptoms of venous thromboembolic disease since risk higher than normal population
The risk of VTE is highest in the acute stage of
spinal cord injury, which coincides, with the period
of flaccid paralysis. Muscular spasticity and lower
limbs muscle spasms usually develop within
months. These could theoretically prevent venous
stasis and contribute to more effective emptying
of lower extremity veins by improving the efficacy
of the calf muscle pump [4,6].
The vascular changes in the paralysed lower limbs
are well documented. There is a generalized
atrophy of the arteries and reduced blood flow
to the paralyzed lower limbs, which represents
adaptations to a lower oxygen demand as a consequence
of reduced activity of the paralyzed
muscles [14]. This process is usually well established
within 6 weeks of onset of the lower limbs
paralysis [15]. This vascular atrophy will lead to
reduction of the blood flow in the calf veins
resulting in shrinkage of the veins size and dispensability
[16]. This process will subsequently
reduce the stasis and pooling of the blood that
usually happen after sudden onset of paralysis
and is the major factor for the development of
VTE.
Several circumstantial evidence point out to the
low risk of VTE in long term immobile patients
whether their lower limbs paralysis is spastic or not.

19. Urinary Tract Dysfunction

20. Urinary Tract Dysfunction
Anatomy:
Internal sphincter:
junction of the bladder neck and proximal urethra
Functional sphincter: progressive increase in tone with bladder filling
Autonomic control: sympathetic alpha-receptors
External sphincter:
Somatic innervation (pudental n. S2-4)
In males, is at the level of the membraneous urethra
Traditionally, the urethra has been thought to
have two distinct sphincters, the internal and the
external, or rhabdosphincter. The internal sphincter
is not a true anatomic sphincter. Instead, in
both males and females, the term refers to the
junction of the bladder neck and proximal urethra,
formed from the circular arrangement of connective
tissue and smooth muscle fibers that extend
from the bladder. This area is considered to be a
functional sphincter because there is a progressive
increase in tone with bladder filling so that the
urethral pressure is greater than the intravesical
pressure. These smooth muscle fibers also extend
submucosally down the urethra and lie above the
external sphincter. The internal urethral sphincter
has been described as being under the control of
the autonomic system. This area has a large number
of sympathetic alpha-receptors, which cause
closure when stimulated.
The external urethral sphincter has somatic
innervation from the sacral region (S2–S4) via the
pudendal nerve, allowing the sphincter to be
closed at will. In males, the external sphincter has
the bulk of the fibers found at the membranous
urethra, but fibers also run up to the bladder neck.
In females, striated skeletal muscle fibers circle the
upper two-thirds of the urethra. In non-SCI individuals,
it is under voluntary control.
Changes frequently occur after SCI. In those
with SCI, the distinction between the internal and
external sphincter becomes less clear. There may
be substantial invasion of the alpha-adrenergic
nerve fibers in the smooth and striated muscle in
the urethra of individuals with SCI with lower
motor neuron lesions. Moreover, those with SCI
frequently do not have control of their external
sphincter. If the sphincter does not relax when the
bladder is relaxing (detrusor sphincter dyssynergia),
high pressures often build in the bladder,
which can affect kidney drainage. In those with
sacral injuries, there may be less ability of the
sphincter to contract, allowing urinary incontinence
to occur. This will be discussed further
when discussing the various types of SCI.

21. Urinary Tract Dysfunction
Physiology:
Bladder contraction:
Parasympathetic efferent via pelvic nerves from sacral cord at S2-4
Outlet resistance and Storage
Preganglionic Sympathetic efferent originate at T11-L2, then travel through the sympathetic paravertebral ganglia
Postganglionic fibers in the hypogastric nerves activate alpha- and beta-adrenergic receptors within the bladder and urethra
The parasympathetic efferent (motor) supply
originates from the sacral cord at S2–S4. Sacral
efferents travel via the pelvic nerves to provide
excitatory input to the bladder. Parasympathetic
bladder receptors are called cholinergic because
the primary postganglionic neurotransmitter is
acetylcholine. These receptors are distributed
throughout the bladder. Stimulation causes a bladder
contraction.
The sympathetic efferent nerve supply to the
bladder and urethra begins in the intermediolateral
gray column from T11 through L2 and provides
inhibitory input to the bladder. Sympathetic impulses
travel a relatively short distance to the lumbar
sympathetic paravertebral (sympathetic) ganglia.
From here the sympathetic impulses travel over
long postganglionic fibers in the hypogastric nerves
to synapse at alpha- and beta-adrenergic receptors
within the bladder and urethra. The primary postganglionic
neurotransmitter for the sympathetic
system is norepinephrine.
Sympathetic efferent stimulation facilitates
bladder storage. This is because of the strategic
location of the adrenergic receptors. Beta-adrenergic
receptors predominate in the superior portion
(i.e., body) of the bladder. Stimulation of betareceptors
causes smooth muscle relaxation so the
bladder wall relaxes. Alpha-receptors have a higher
density near the base of the bladder and prostatic
urethra; stimulation of these receptors causes
smooth muscle contractions of the sphincter and
prostate, which increases the outlet resistance of
the bladder and prostatic urethra.
Beta-receptors: produce smooth muscle relaxation of the bladder wall
Alpha-receptors: high density at the internal sphincter and prostatic urethra increases outlet resistance

22. Urinary Tract Dysfunction
Voiding Centers
Sacral Micturation Center: Afferent impulses provide info regarding bladder fullness. Reflexive parasympathetic impulses to the bladder cause bladder contraction
Pontine Micturation Center: coordinates external sphincter relaxation when the bladder contracts (Detrusor Sphincter Dyssynergia)
Cerebral cortex: voluntary inhibition of the sacral micturation center [Suprasacral SCI=involuntary (uninhibited) bladder contraction]
Voiding Centers
Facilitation and inhibition of voiding is under
three main centers, the sacral micturition center,
the pontine micturition center, and the higher centers
(cerebral cortex).
The sacral micturition center (S2–S4) is primarily
a reflex center in which efferent parasympathetic
impulses to the bladder cause a bladder
contraction, and afferent impulses to the sacral
micturition center provide feedback regarding
bladder fullness.
The pontine micturition center is primarily
responsible for coordinating relaxation of the urinary
sphincter when the bladder contracts.
Suprasacral SCI disrupts the signals from the pontine
micturition center, which is why detrusor
sphincter dyssynergia is common in those with
suprasacral SCI.
The net effect of the cerebral cortex on micturition
is inhibitory to the sacral micturition center.
Because suprasacral SCI also disrupts the
inhibitory impulses from the cerebral cortex, those
with suprasacral SCI frequently have small bladder
capacities with involuntary (uninhibited) bladder
contractions.

23. Urinary Tract Dysfunction
Voiding Dysfunctions:
Suprasacral Spinal Cord Lesions
Initial period of spinal shok resulting in detrusor areflexia
Uninhibited bladder contractions
Detrusor-external sphincter dyssynergia: Occurs in 96% of individuals with suprasacral lesions
Autonomic dysreflexia (T6 or above): exaggerated response to noxious stimuli that provokes uninhibited bladder contractions and sphincter dyssynergia
Sacral Lesions
Detrusor areflexia: result in highly compliant acontractile bladder
Normal or underactive external sphincter resulting in dyssynergy or coordination, respectively.
SUPRASACRAL SPINAL CORD LESIONS
Traumatic suprasacral SCI results in an initial
period of spinal shock, during which there is
detrusor areflexia. During this phase, the bladder
has no contractions. The neurophysiology for
spinal shock and its recovery is not known. Recovery
of bladder function usually follows recovery of
skeletal muscle reflexes. Uninhibited bladder contractions
gradually return after 6 to 8 weeks.
Clinically, a person with a traumatic
suprasacral SCI may begin having episodes of urinary
incontinence and various visceral sensations,
such as tingling, flushing, increased lower extremity
spasms, or autonomic dysreflexia with the onset
of uninhibited contractions. As uninhibited bladder
contractions become stronger, the post-void residuals
(PVRs) decrease. Eventually these individuals
develop uninhibited contractions Unfortunately,
high intravesical voiding pressures usually are
required for the development of a balanced bladder.
It has been found that high voiding pressures
and prolonged duration of the bladder contractions
may cause hydronephrosis and renal deterioration.
Urodynamic studies are used to determine these
voiding parameters.
Detrusor-external sphincter dyssynergia
(DESD) also commonly occurs following
suprasacral lesions. DESD is defined as intermittent
or complete failure of relaxation of the urinary
sphincter during a bladder contraction and
voiding. It has been reported to occur in 96 percent
of individuals with suprasacral lesions. In
addition to DESD, internal sphincter dyssynergia
also has been reported, often occurring at the
same time as detrusor-external sphincter dyssynergia.
In this guideline the term detrusor sphincter
dyssynergia will be used throughout to refer to the
entire sphincter mechanism—internal and external
sphincter.
SACRAL LESIONS
A variety of lesions can affect the sacral cord
or roots. Damage to the sacral cord or roots generally
results in a highly compliant acontractile
bladder; however, particularly in individuals with
partial injuries, the areflexia may be accompanied
by decreased bladder compliance resulting in progressive
increases in intravesical pressure with filling
(Herschorn and Hewitt, 1998). The exact
mechanism by which sacral parasympathetic
decentralization of the bladder causes decreased
compliance is unknown.
It has been noted that the external sphincter is
not affected to the same extent as the detrusor.
This is because the pelvic nerve innervation to the
bladder usually arises one segment higher than the
pudendal nerve innervation to the sphincter. Also,
the nuclei are located in different portions of the
sacral cord, with the detrusor nuclei located in the
intermediolateral cell column and the pudendal
nuclei located in the ventral gray matter. This combination
of detrusor areflexia and an intact sphincter
helps contribute to bladder overdistention and
decompensation.
AUTONOMIC DYSREFLEXIA
Autonomic dysre.exia is an exaggerated
sympathetic response to a noxious stimulus that occurs below the
level of lesion in injuries at T6 or above. It is caused by lack of descending
supraspinal inhibitory control and can be triggered by any bladder stimulus,
such as overdistension, di.cult catheterization, or even urodynamic studies.
Autonomic dysreflexia is another term mentioned
throughout this guideline. Autonomic dysreflexia
can occur in individuals who have a spinal
cord injury at thoracic level 6 (T6) or above. It
occurs as a result of any noxious stimuli. The most
common causes are bladder distention (which provokes
uninhibited bladder contractions and sphincter
dyssynergia) and bowel problems such as
constipation and impaction.
The most dramatic problem associated with
autonomic dysreflexia is a sudden severe elevation
in blood pressure. Those with an SCI at or above
T6 frequently have a normal systolic blood pressure
in the 90–110 mm Hg range. Autonomic dysreflexia
is frequently defined in adults as a systolic
blood pressure greater than 140 mm Hg. Another
definition is a systolic blood pressure 20 to 40 mm
Hg above baseline. Systolic blood pressures elevations
more than 15–20 mm Hg above baseline in
adolescents with SCI or more than 15 mm Hg
above baseline in children may be a sign of autonomic
dysreflexia.

24. Urinary Tract Dysfunction
The majority of patients with SCI have voiding dysfunction (Consortium for Spinal Cord Medicine 2006)
Renal diseases were the main cause of mortality in spinal cord injured patients prior to the WWII and the Korean war (Jamie 2001)
Management goals for prevention of urogenic complications (Samson 2007)
Ensure social continence for reintegration into community
Allow low-pressure storage and efficient bladder emptying at low detrusor pressures
Avoid stretch injury from repeated overdistension
Prevent upper and lower urinary tracts complications from high intravesical pressures
Prevent recurrent urinary tract infections
In the past, renal failure was the leading cause of death after spinal cord injury (SCI). Today mortality from SCI has declined dramatically partly owing to the improved management of urologic dysfunction associated with SCI. The goals of bladder management in spinal cord injury patients are intended to (1) ensure social continence for reintegration into community, (2) allow low-pressure storage and efficient bladder emptying at low detrusor pressures, (3) avoid stretch injury from repeated overdistension, (4) prevent upper and lower urinary tracts complications from high intravesical pressures, and (5) prevent recurrent urinary tract infections. This article provides an overview of neurogenic bladder dysfunction associated with SCI and current management options.

25. Bladder Management
Management method used is based on urodynamic studies
Acute management: indwelling catheter followed by clean intermittent catherization
Longterm management depends on many factors, including the level and completeness of injury, amount of hand function, sex, and motivation.
Clean intermittent catheterization (CIC):
considered the best and safest long-term bladder management method (Samson 2007)
Indwelling catheter:
For patients with limited hand function or lack of motivation to perform CIC.
Increased risk for urinary tract infections; urethral diverticula; urethral strictures; urethritis; traumatic hypospadias; bladder calculi; small, low compliance, high-pressure bladder; and bladder cancer
Crede and Valsalva maneuvers (Samson 2007):
Useful in areflexic bladders with impaired detrusor contraction
Works by increasing intraabdominal pressure or applying direct suprapubic pressure. May be time consuming.
May exacerbate haemorrhoids, hernias, vesico-ureteric reflux and dyssynergia
The high
rate of urologic complications that were once observed with chronic indwelling
catheters are no longer as prevalent because of the routine use of CIC [25].
Chronic indwelling catheters (ie, Foley and suprapubic tubes) have often been
shown to be associated with high rates of chronic urinary tract infections,
urethritis, prostatitis, bladder stones, bladder diverticulae, strictures, abscesses,
bladder cancer, and upper urinary tract disease such as pyelonephritis.
Lapides and colleagues [26] suggest that urinary tract infectious disease is
based on overdistension of the bladder from urinary retention caused by
ischemic changes in the bladder wall that then break down the tissue’s defense
mechanism against infection. Based on this theory, urinary retention,
as opposed to catheterization per se, is the culprit for urinary tract infection.
Intermittent catheterization would therefore prevent overdistension while
.ushing bacterial organisms from the bladder.
and can therefore interfere with work or leisure
activities. Crede manoeuvre and Valsalva manoeuvres
may exacerbate haemorrhoids, hernias and vesico-
ureteric re¯ux and are therefore, usually only suitable
for patients who are unable to do CIC and who have
weak urethral sphincter such as SCI male patients with
lower motor neurone lesions. Valsalva manoeuvre, may
worsen the dyssynergia (DESD).18

26. Bladder Management Reflex voiding: Pharmacological management:
Consist of suprapubic tapping to stimulate the bladder
Useful in patients with Suprasacral lesions with intact sacral reflex arc, in the absence of dyssynergy
May require requires transurethral sphincterotomy
Pharmacological management:
Anticholinergic agents to prevent detrusor overactivity in patients practicing CIC
Intravesical therapy (Samson 2007)
Injection of botulin toxin in the detrusor musculature
Length of action between weeks
Effect: suppression of bladder overactivity, increase in cystometric and maximum bladder capacity, decrease in voiding pressure, and elimination of urinary incontinence that may be associated with detrusor overactivity
Injection into the external urethral sphincter is also used to treat neurogenic detrusor-sphincter dyssynergia

27. Bladder Management Condom catheter: Surgical management:
used for incontinence in males to promote dry perineum
Surgical management:
When primary bladder management methods fail
Electrical stimulation and posterior sacral root rhizotomy
Augmentation cystoplasty, cutaneous conduits, and urinary diversions
Transurethral sphincterotomy: for bladder outlet obstruction and Detrusor Sphincter Dyssynergia
Electrical stimulation and posterior sacral root rhizotomy
In spinal cord injuries from suprasacral lesions, electrical stimulation of
sacral anterior nerve roots has been used to produce e.ective micturition
with relatively low residual volumes. Electrodes are surgically implanted on
sacral nerves with the stimulator placed under the skin, generally the abdomen.
Stimulation is provided directly to the S3 nerve root and suppresses
hyperre.exic detrusor activity. This mechanism is often combined with
division of the posterior sacral roots and is intended to eliminate detrusor
and sphincter hyperre.exia, increase bladder capacity and compliance,
and decrease incidence of re.ex incontinence.
Various other forms of surgical continence measures are available when
primary bladder management methods fail. These include augmentation cystoplasty
and various cutaneous conduits/urinary diversion methods wherein
the ureters are connected to an intestinal segment that is externalized through
the abdominal wall, draining into an external collecting device. Urinary diversions
are sometimes performed in women who have di.culty performing
catheterization and patients who have complications caused by indwelling
catheters, perineal decubiti, and bladder malignancy requiring cystectomy.
The goal of bladder augmentation (or augmentation enterocystoplasty) is
to increase total bladder capacity. In patients who have SCI with neurogenic
bladder dysfunction refractory to conservative management, this procedure
is intended to increase detrusor compliance and lower bladder storage pressures
that may place the upper tracts at risk for deterioration [42]. The basic
procedure involves using a bowel segment, such as the ileum, right colon,
descending/sigmoid colon, or stomach, to augment the bladder (Fig. 4). It
is an irreversible procedure and should be used for patients who have undergone
failed conservative medical management in the setting of high detrusor
pressures. An alternative surgical approach is detrusor myomectomy
through excision of the submucosa, creating a weakened muscle and resultant
diverticulum [43]. An alternative surgical approach is detrusor myomectomy
through excision of the submucosa, creating a weakened muscle and
resultant diverticulum [43]. In most cases, spontaneous voiding after surgery
will likely not occur, and permanent intermittent catheterization is the
norm. Long-term complications, most notably metabolic derangements
and change in bowel habits, depend on the segment of bowel used.
Diverting the urine from the LUT and perineum might become necessary
for some patients who have SCI who have di.culties with catheterization,
have urethral or penile skin changes such as .stulae or strictures, or experience
incontinence that impairs management of decubitus ulcers [44]. Supravesical
conduits or continent diversions using a bowel segment are
performed when a bladder neck closure or suprapubic tube placement is
not an option [44]. The simplest surgical method is the ileal conduit. In
this method, an adequate length of bowel segment is resected, the ureters
are implanted at the proximal end of this segment, and the distal end is
externalized through the abdominal wall. Subsequent urostomy care is
performed with relative ease as opposed to a continent stoma. This conduit
is not a urine storage reservoir; there is only transient contact of urine with
the absorptive surface, and therefore no signi.cant metabolic derangement
is seen compared with other forms of surgical bladder management. Continued
routine monitoring of basic metabolic pro.le, renal function, and the
upper tracts for deterioration is required.
Transurethral sphincterotomy
Transurethral sphincterotomy is the transurethral surgical incision of the
external urinary sphincter in cases of bladder outlet obstruction secondary
to DESD, allowing subsequent use of an external collecting device. This
procedure has been mainstay of treatment for signi.cant DESD with associated
elevated detrusor voiding pressure unresponsive to anticholinergic
agents. The decrease in outlet resistance theoretically lowers the high detrusor
pressures associated with DESD and averts the need for an indwelling
catheter. It is typically performed in male quadriplegic or high-thoracic
paraplegic patients who have di.culties performing CIC secondary to poor
hand function.

28. Bladder Management Complications of neurogenic bladder
chronic urinary tract infections, bladder diverticulae, bladder stones, urethral trauma leading to penile fistulae or strictures, perineal decubiti, bladder cancer, vesicoureteral reflux, hydronephrosis, pyelonephritis, and renal failure
It is not recommended to give prophylactic antibiotics or to treat asymptomatic bacteriuria (Samson 2007)
Treatment
of asymptomatic bacteriuria or prophylactic use of antibiotics is not usually
recommended

29. Shoulder Arthropathies

30. Shoulder Arthropathies
Prevalence of shoulder pain in paraplegic individual has been reported to be between 30% and 70% (Alm 2008)
In paraplegic patients, the shoulder becomes weight bearing and is overused
The use of manual wheelchair contributes to the high incidence of shoulder arthropathies due to the significant stability and mobility demands it places on the shoulder
Neuromuscular fatigue leads to decreased stability and superior displacement of the humeral head
Common pathologies include:
Chronic inflammation (especially supraspinatus)
Impingement syndrome
Bursitis
Rotator cuff tears
Bicipital tendinitis
Glenohumeral and acromioclavicular arthritis
Peripheral neuropathies (carpal tunnel syndrome) are also common
Manual WC use places significant stability and mobility
demands on the upper limbs and is thought to contribute
to the high incidence of upper extremity pain and injury,
particularly at the shoulder. Because individuals with SCI
are dependent on their upper extremities for both
functional mobility and activities of daily living, shoulder
joint pain can present a devastating loss of function and
independence (2–4) and decreased quality of life (5,6).
During WC propulsion, anatomical structures in the

31. Shoulder Arthropathies
Gutierrez et al. (2007) demonstrated that paraplegic patients with higher levels of shoulder pain reported lower subjective quality of life and physical activity scores
Interventions:
Designing ergonomic ways for patients to transfer
Wheelchair biomechanics (power)
Physiotherapy to enhance shoulder stability
Core body support for patients with high thoracic paraplegia
Medical management
Surgical management (cuff repair, subacromial debridement, shoulder arthroplasty)
Conclusions: Persons with SCI who reported lower subjective quality of life and physical activity scores
experienced significantly higher levels of shoulder pain. However, shoulder pain intensity did not relate to
involvement in general community activities. Attention to and interventions for shoulder pain in persons
with SCI may improve their overall quality of life and physical activity.

32. Pulmonary Complications

33. Pulmonary Complications
Leading cause of mortality in the first year following SCI (Wuermser et al. 2007)
Primary contributors:
Difficulty handling secretions
Atelectasis
Hypoventilation
Weak or paralyzed abdominal muscles preclude an effective cough.
Vital capacity declines in high paraplegia from respiratory muscle weakness, can lead to a restrictive ventilatory deficit
The primary contributors to pulmonary dysfunction after
SCI are difficulty handling secretions, atelectasis, and hypoventilatio
After SCI, a restrictive ventilatory deficit occurs and there is
a resultant decrease in all lung volumes. Vital capacity (VC)
declines in tetraplegia and high paraplegia from respiratory
muscle weakness.

34. Pulmonary Complications
(Schilero et al 2009)

35. Pulmonary Complications
(Schilero et al 2009)

36. Pulmonary Complications
Recent findings suggest that expiratory muscle training, electrical stimulation of expiratory muscles and administration of a long acting Beta2-agonist (salmeterol) improve physiological parameters and cough. (Schilero et al 2009)
Prompt treatment of infectious pulmonary diseases is required.

37. Neurogenic Heterotopic Ossification

38. Neurogenic Heterotopic Ossification
Incidence ranges from 10% to 53%
Generally manifests 1 to 6 months post-injury but may develop several years after SCI
Occurs below the level of SCI most commonly affecting the hips
Common clinical findings:
Decreased ROM, peri-articular swelling, erythema, and warmth, pain (in patients with sensory sparing), low grade fever, spasticity
NHO originates in connective tissues
Factors associated with NHO (van Kuijk et al. 2002):
Completeness of SCI, presence of pressure sores, UTI (immunogenic), DVT, severe spasticity and trauma
Although NHO may develop even several years
after SCI, it is generally diagnosed between 1 to 6
months post-injury with a peak incidence at 2
months7,8,10,12,19,22,45 ± 50 Although NHO may begin
SCI.3,4,7,9,39,51 The most common clinical ®ndings are
a decreased joint range of motion and a peri-articular
swelling due to interstitial oedema of the soft
tissues.1,7,8,10,30,36,39,45,52,53 In patients with sensory
sparing, the ®rst symptom may be pain in the a€ected
area.10,54 Peri-articular erythema and warmth may also
occur, sometimes accompanied by a low-grade fever.55
Spasticity may increase secondary to the NHO
development.53 Reduction of hip joint movement and
spasticity may lead to loss of an adequate sitting
position,51 pressure sores, and related pain com-
plaints52 and may also compromise transfers and
activities of daily living. Although not commonly
reported in SCI patients, ectopic ossi®cation has been
associated with compression of vascular structures and
nearby peripheral nerves.56 ± 61 The relatively low
or retain ambulation.
Other clinical factors associated with NHO are the
presence of pressure sores,6,21,22,24,30,47 urinary tract
infections or renal stones,3,4,6,24,100 deep venous
thrombosis (DVT),24 severe spasticity,22 and (micro)
trauma. An area of soft tissue damage due to pressure
ulceration with subsequent oedema may predispose to
the development of ectopic ossi®cation.101 On the
other hand, pressure sores may occur secondary to
NHO due to a decrease in eg hip range of motion that
a€ects sitting position and alters pressure patterns. As
a result, body weight is unequally distributed among
the tubera and pressure ulceration may evolve, mostly
contralateral to the NHO a€ected side.11
An infected urinary tract could serve as a source of

39. Neurogenic Heterotopic Ossification
Primary prevention:
Controlling contributing factors: pressure sores, trauma, UTI, and DVTs.
Gentle ROM exercises to prevent ankylosis; avoid rigorous exercise which can induce microtrauma
Early identification and appropriate treatment
No controlled trials exist on the prophylactic use of NSAID, diphosphonates, and irradiation in the prevention of heterotopic ossification in SCI patients.
Various, more speci®c prophylactic measures have
been proposed to prevent NHO, including the use of
diphosphonates, NSAID, and more recently irradia-
tion. The latter two methods have been successful to
some degree in preventing heterotopic ossi®cation eg
after THA,142,152,153,160 ± 163,180 but no controlled
studies are available in SCI patients.

40. Spasticity

41. Spasticity Part of the upper motor neuron syndrome
Commonly affects antigravity muscles; in the lower limbs, the extensors are most often affected.
Amongst patients with chronic SCI, 65–78% report symptoms of spasticity; and 37% of them require treatment. (Craven 2009)
Mainstays of treatment
Avoiding triggers: UTIs, constipation, bladder distention
Therapy: hot or cold application, stretching, positioning and splinting to prevent contracture
Pharmacological treatment: A recent review has supported the efficacy of baclofen, tizanidine, clonidine, cyproheptadine, gabapentine and L-threonin, in reducing spasticity following SCI (Crave 2009)
Neurosurgical procedure
muscle spasms. On the other hand, excessive muscle spasms
in the lower-extremity extensor muscles are prominent
following SCI. It is also believed that the mechanisms underlying
spasticity in stroke and SCI are different. Neural
Amongst patients with chronic SCI (41 year after injury),
65–78% report symptoms of spasticity; and 37% whom
require treatment.11,12 One of the greatest challenges facing
the SCI clinician and rehabilitation team is evaluating the
effectiveness of drug and/or rehabilitation interventions
intended to ameliorate spasticity. The mainstays of treatment
for spasticity include rehabilitation therapies such as
hot or cold application, stretching, positioning and splinting
to prevent contracture, in addition to oral and or injectable
pharmacologic treatments and neurosurgical procedures.
A recent evidence-based review of current interventions
indicated that several pharmacalogical agents (baclofen,
tizanidine, clonidine, cyproheptadine, gabapentine and
L-threonin) and transcutaneous electrical nerve stimulation
had good to excellent levels of evidence of their efficacy for
reducing spasticity after SCI.13,14 A prior systematic review of
the comparative and efficacy and safety of skeletal muscle
relaxants for treatment of spasticity among patients with
diverse neurologic impairments revealed equivalent efficacy
of baclofen and tizanidine with a higher frequency of dry
mouth with tizanidine and more weakness with baclofen.15
A recent systematic review of stretching efficacy indicated
inconclusive evidence regarding its efficacy for spasticity
reduction.16 Quantitative assessment of spasticity (both
relative and absolute) is vital to the detection of spasticity
among individuals with SCI and determination of treatment
efficacy in a clinical trial setting or effectiveness in the clinic
setting. A reliable tool to quantify lower extremity spasticity
is needed.

42. Bowel complications

43. Bowel complications
Continence is maintained by the resting tone and reflex activity of the internal anal sphincter, external anal sphincter and muscles of the pelvic floor
Reflex contraction of the external anal sphincter complex on coughing and valsalva prevents incontinence
Rectal distension triggers the rectoanal inhibitory reflex, where the internal anal sphincter relaxes. In this situation, voluntary contraction of the external anal sphincter is required to retain continence
Enteric nervous system (intrinsic) coordinate gut motility
Extrinsic nervous system modulates the activity of the enteric nervous system and coordinate gut activity to systemic demands
Continence is maintained by the resting tone and
re¯ex activity of the IAS, EAS and muscles of the
pelvic ¯oor. The resting anal canal pressure is
maintained by tonic contraction of the IAS. Re¯ex
contraction of the EAS complex on coughing or
Valsalva prevents leakage by kinking the anal canal
in opposing directions. Rectal distention produces
stretching of the puborectalis and the urge to
defecate. The distended rectum causes re¯ex relaxa-
tion of the IAS (rectoanal inhibitory re¯ex (RAIR))
resulting in faeces reaching the upper anal canal
where receptors sample the rectal contents. Then
voluntary EAS contraction maintains continence by
mechanically sealing the rectal neck and mechani-
cally preventing further relaxation of the IAS.
Defecation is a coordinated event requiring simulta-
neous relaxation of the puborectalis to widen the
anorectal angle, relaxation of the EAS, and rectal
contraction.
). Sympathetics are inhibitory and function to
ecrease bloow ¯ow and slow motility by relaxing
he colonic wall to increase compliance. Sympathetic
nerves and from the inferior mesenteric ganglion
through the hypogastric nerves. The sympathetic effect
is excitatory, and tonic discharge maintains IAS
closure. With rectal distension or digital stimulation,

44. Bowel complications
Parasympathetic activity through the pelvic nerves (pelvic plexus S2-4) causes smooth muscle contraction, which promotes gut motility. It also leads to internal anal sphincter relaxation
Sympathetics (T9-10) are inhibitory and function to decrease blood flow and slow motility by relaxing the colonic wall to increase compliance
The sympathetic effect is excitatory, and tonic discharge maintains IAS closure
The external anal sphincter is a striated muscle innvervated from the sacral cord via the pudendal nerves (S2-S4).

45. Bowel complications (Lynch 2001)
supraconal injury:
results in loss of conscious sphincter control
Anorectal dyssynergy: Spastic EAS
Manual stimulation: rectoanal inhibitory reflex (result in relaxation of IAS, EAS, and triggers peristalsis)
Manual evacuation: If unable to relax EAS
The level of the spinal cord lesion determines the
e€ect on colonic motility. A supraconal (Upper Motor
Neuron or UMN) SCI results in loss of conscious
sphincter control and an inability to signi®cantly
increase intraabdominal pressure. There is a loss of
voluntary control of defecation and a degree of
anorectal dyssynergy. This means that straining and
rectal contraction result in increased tone in the EAS.
Loss of rectal sensation and a spastic EAS require
defecation to be anticipated. Re¯ex defecation can be
initiated by mucosal stimulation, either digitally or
with a suppository. Stimulation activates the rectoanal
inhibitory re¯ex. It can be exploited to cause
relaxation of the IAS, re¯ex relaxation of the EAS
and pelvic nerve mediated peristalsis. If there is no
re¯ex relaxation of the EAS complex, re¯ex evacuation

46. Bowel complications (Lynch 2001)
Cauda equina injuries
EAS and pelvic muscles become flaccid (loss sympathetic tone and voluntary contraction)
Loss of parasympathetic control and reflex innervation to IAS result in decreased resting anal tone
Valsalva results in incontinence when rectum full
LMN injury from a lesion affecting the conus, cauda equina or pelvic nerves results in interruption of the parasympathetic supply to the colon and reduced spinal cord-mediated reflex peristalsis.
Lesions above T1 result in delayed mouth-to-caecum time
Patients with thoracic spine injury show abnormal response to increasing intestinal volumes which suggests that the CNS is necessary to modulate colonic motility
The lack of compliance leads to functional obstruction, increased transit times, and abdominal distension, bloating and discomfort
Complete or partial injuries to the cauda equina
result in a lower motor neuron (LMN) pattern of
injury. The EAS and pelvic muscle are ¯accid and
there is no re¯ex response to increased intraabdominal
pressure. The loss of parasympathetic control and
re¯ex innervation of the IAS means a further
reduction in resting anal tone and leads to faecal
incontinence. A person with a LMN lesion following
SCI will have absent EAS tone and decreased re¯ex
peristalsis. Valsalva can result in faecal leakage and
the rectum has to be kept empty to avoid faecal
incontinence. Stool has to be removed digitally,
assisted by Valsalva and abdominal massage.
di€erent levels and degrees of SCI. Lesions above T1
result in delayed mouth-to-caecum time, but lesions
are markedly delayed. A LMN injury from a lesion
a€ecting the conus, cauda equina or pelvic nerves
results in interruption of the parasympathetic supply
to the colon and reduced spinal cord-mediated re¯ex
peristalsis. Stool propulsion is by segmental colonic
The delay in transit may in part be due to loss of
colonic compliance. The colon of patients with complete
thoracic injury has been shown to have an abnormal
response to increasing volume. Distension with water to
generate a volume/pressure curve (colometrogram)
produces a hyperre¯exic response similar to that
described in the bladder.34 With a spinal cord lesion
above L1, the left colon is less compliant. Above T5, the
right colon is also a€ected. The lack of compliance leads
to functional obstruction, increased transit times, and
abdominal distension, bloating and discomfort. It
suggests that the CNS is necessary to modulate colonic
motility.35 Colonic myoelectric activity has been

47. Bowel complications
Colorectal dysfunction is a common problem affecting approximately 80% of patients.
Important long term implications for quality of life
Complications: obstruction, diverticulosis, bloating, incontinence, psychosocial
Bowel care regimen: bowel evacuation to prevent incontinence or impaction
Dietary manipulation: water and fibers to promote transit and soft stools
Stool softeners: prevents constipation and potential for autonomic dysreflexia
Prokinetic agents
Enemas
Digital stimulation: triggers rectoanal inhibitory reflex (relax IAS). Usefull in patients with UMN lesions.
Manual removal: LMN lesions and Anorectal dyssynergy
Colostomy

48. Neuropathic pain
Prevelance of pain in patients with SCI is around 65-85%, 1/3 of which have severe pain (Siddall 2009)
Poor prognosis
Pharmacological (pain clinic)
Surgical
following SCI is common. Although there is some variability,
studies investigating the prevalence of pain in people with
SCI indicate that around 65–85% of those with a spinal
injury will experience pain and around one-third of these
will have severe pain.1

49. Cardiovascular Complications
Autonomic dysreflexia:
sudden severe elevation in blood pressure
Orthostatic hypotension
Coronary Diseases

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